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Anxiety disorders are a significant problem in the community, and recent neuroimaging research has focused on determining the brain circuits that underlie them. Research on the neurocircuitry of anxiety disorders has its roots in the study of fear circuits in animal models and the study of brain responses to emotional stimuli in healthy humans. We review this research, as well as neuroimaging studies of anxiety disorders. In general, these studies have reported relatively heightened amygdala activation in response to disorder-relevant stimuli in post-traumatic stress disorder, social phobia, and specific phobia. Activation in the insular cortex appears to be heightened in many of the anxiety disorders. Unlike other anxiety disorders, post-traumatic stress disorder is associated with diminished responsivity in the rostral anterior cingulate cortex and adjacent ventral medial prefrontal cortex. Additional research will be needed to (1) clarify the exact role of each component of the fear circuitry in the anxiety disorders, (2) determine whether functional abnormalities identified in the anxiety disorders represent acquired signs of the disorders or vulnerability factors that increase the risk of developing them, (3) link the findings of functional neuroimaging studies with those of neurochemistry studies, and (4) use functional neuroimaging to predict treatment response and assess treatment-related changes in brain function.
(Reprinted with permission from Neuropsychopharmacology Reviews 2010; 35:169–191)
Anxiety disorders are marked by excessive fear (and avoidance), often in response to specific objects or situations and in the absence of true danger, and they are extremely common in the general population. According to a recent epidemiological study, the lifetime prevalence of any anxiety disorder is 28.8% (Kessler et al, 2005). Anxiety disorders are associated with impaired workplace performance and hefty economic costs (Greenberg et al, 1999), as well as an increased risk of cardiovascular morbidity and mortality (Albert et al, 2005; Kawachi et al, 1994; Smoller et al, 2007). Given that anxiety disorders are a significant problem in the community, recent neuroimaging research has focused on determining the brain circuits that underlie them to inform the use of existing treatments and guide the possible development of new treatments. In the future, neuroimaging studies of anxiety disorders may also prove to be clinically helpful in the prediction of treatment response.
Given that excessive fear is a key component of anxiety disorders, it is not surprising that the search for the neurocircuitry of anxiety disorders has its roots in and has been closely intertwined with studies of fear circuits in animal models. A large volume of experimental work has examined the neurocircuitry associated with fear responses, mainly in rodents, using primarily fear conditioning, inhibitory avoidance, and fear-potentiated startle models. Key components of fear circuitry including the amygdala (and its subnuclei), nucleus accumbens (including bed nucleus of stria terminalis BNST), hippocampus, ventro-medial hypothalamus, periaqueductal gray, a number of brain stem nuclei, thalamic nuclei, insular cortex, and some prefrontal regions (mainly infralimbic cortex) have been identified in these studies (for recent reviews see Davis, 2006; Maren, 2008; Quirk and Mueller, 2008). These regions have their respective roles in the various components of fear processing such as the perception of threat or of unconditioned stimuli, the pairing of an unconditioned stimulus and conditioned response (learning/conditioning), the execution of efferent components of fear response, and the modulation of fear responses through potentiation, contextual modulation, or extinction. Some key findings from animal literature, such as the central role of amygdaloid nuclei in the acquisition of fear conditioning and expression of fear responses, the involvement of the hippocampus in contextual processing, and the importance of the infralimbic cortex in extinction recall, have been replicated across different studies and laboratories. These basic components of fear circuitry are well preserved across species and likely support similar functions in humans. Animal work using in vivo electrophysiological recording, tracing and lesions/reversible inactivation techniques was indispensable in acquiring this knowledge. Some recent work had even suggested that there might be separate fear and anxiety systems orchestrated through the central nucleus of the amygdala and the BNST, respectively (Davis, 2006). These types of findings are particularly exciting as they might allow for a better focus on the neurocircuits involved in pathological anxiety.
On the other hand, other important issues, such as the exact neuroanatomical region that stores fear memory traces, or the exact role of a particular process (eg, the role of reconsolidation in fear memory, Nader and Hardt, 2009), or of a particular region (eg, the insular cortex) are intensely debated and actively studied. Nevertheless, the basic fear-related neurocircuitry identified in rodents is a useful place to start examining anxiety-related neurocircuitry in humans. It is important to note that the exact roles of many brain regions are yet to be firmly established and could differ across species. Even regions such as the amygdala, hippocampus, and nucleus accumbens might be involved in different, additional, or even unique tasks in humans (eg, the role of the hippocampus in explicit verbal memory in humans). Finally, there are major differences between human anxiety/anxiety disorders and fear conditioning models in animals. These differences include the frequent absence of clear unconditioned stimuli (US) in human anxiety disorders, and the central roles of avoidance and cognitive components (eg, anticipatory anxiety) in humans. These unique characteristics of anxiety disorders suggest potential involvement of other brain regions in addition to those identified in rodents, such as areas of prefrontal cortex that are more unique to humans. Thus, although animal studies are indispensable in understanding basic fear neurocircuitry, in vivo human studies are critical for understanding the neurocircuitry of anxiety disorders.
In this review, we will discuss three main topics: (1) fear neurocircuitry in healthy humans; (2) stress as a normal response to internal and external stimuli, and (3) anxiety disorders as defined in human psychopathology. The first of these topics will include a discussion of Pavlovian fear conditioning and extinction, pharmacologically induced fear and anxiety states, and the assessment of emotional stimuli in humans. In the third topic, we review the role of brain regions such as the amygdala, medial prefrontal cortex (including the rostral anterior cingulate cortex (rACC) and dorsal anterior cingulate cortex (dACC)), hippocampus, and insular cortex in anxiety disorders (Figure 1). Finally, we discuss some of the limitations of neuroimaging studies of anxiety disorders as well as the directions that we expect the field to take in the near future.
Magnetic Resonance Images (Sagittal Slices) Showing the Structures of Interest in This Review: (a) the Hippocampus and the Amygdala; (b) the Dorsal Anterior Cingulate Cortex (dACC) and the Rostral Anterior Cinulate Cortex (rACC); and (c) the Insular Cortex.
In its most basic form, Pavlovian fear conditioning involves repeatedly presenting a previously neutral conditioned stimulus (CS; eg, a tone) with an aversive unconditioned stimulus (US; eg, a shock). After repeated pairings, the CS alone comes to elicit a conditioned fear response (eg, increased freezing, fear-potentiated startle, or skin conductance responses). Pavlovian fear conditioning has been used as a testable and translational, though admittedly simplistic, model of the acquisition of fears that might be relevant to some anxiety disorders like phobias and possibly to some aspects of post-traumatic stress disorder (PTSD).
Studies of Pavlovian fear conditioning in non-humans have highlighted the importance of the amygdala in the acquisition of fear conditioning (LeDoux, 2000; LeDoux et al, 1990; Pare et al, 2004; Sananes and Davis, 1992). Similarly, functional neuroimaging studies in humans have reported amygdala activation during fear conditioning (Alvarez et al, 2008; Barrett and Armony, 2009; Buchel et al, 1998, 1999; Cheng et al, 2003, 2006; Gottfried and Dolan, 2004; Knight et al, 2004, 2005; LaBar et al, 1998; Milad et al, 2007b; Morris and Dolan, 2004; Pine et al, 2001; Tabbert et al, 2006), even when the CS is presented below perceptual thresholds (Critchley et al, 2002; Knight et al, 2009; Morris et al, 2001) and even when more complex USs are used (Doronbekov et al, 2005; Klucken et al, 2009). In addition, amygdala activity has been associated with skin conductance changes during fear conditioning (Cheng et al, 2006; Furmark et al, 1997; LaBar et al, 1998; Phelps et al, 2001). Interestingly, amygdala activation in humans also has been observed in response to cues following (1) verbal instructions that discriminate between cues that predict shock vs safety (even though no shock was actually administered) (Phelps et al, 2001), and (2) observational fear learning, whereby participants watch a video of another person experiencing a Pavlovian fear-conditioning paradigm (Olsson et al, 2007). What exactly amygdaloid activation represents in these latter paradigms is not entirely clear. It could suggest for example that: (1) higher order centers that decipher the anticipated predictive value of the cue, or that learn from observation using empathy, convey information to the amygdala, or (2) alternatively, that the human amygdala is less specific in its responses and is more sensitive to contextual modulation in the absence of a US. These interpretations could have potentially different implications for the understanding of the role of the amygdala in anxiety disorders.
Fear conditioning is also associated with increased activation in the dACC and rACC (Alvarez et al, 2008; Buchel et al, 1998, 1999; Dunsmoor et al, 2007; Klucken et al, 2009; LaBar et al, 1998; Marschner et al, 2008; Milad et al, 2007a,b; Morris and Dolan, 2004; Phelps et al, 2004). Activation in the dACC and rACC also occurs during observational fear learning (Olsson et al, 2007). In addition, dACC activation is positively correlated with differential skin conductance responses (Milad et al, 2007a). Fear conditioning studies (involving both specific CSs and contexts) also commonly report insular cortex activation (Alvarez et al, 2008; Buchel et al, 1999; Buchel et al, 1998; Critchley et al, 2002; Dunsmoor et al, 2007; Gottfried and Dolan, 2004; Klucken et al, 2009; Knight et al, 2009; Marschner et al, 2008; Morris and Dolan, 2004; Phelps et al, 2001, 2004) and hippocampal activation (Alvarez et al, 2008; Buchel et al, 1999; Knight et al, 2004, 2009; Lang et al, 2009; Marschner et al, 2008).
Extinction learning occurs when a CS that previously predicted a US no longer does so, and over time, the conditioned response (eg, freezing or elevated skin conductance responses) decreases. Extinction learning or, more likely, the later recall of this learning involves the ventromedial prefrontal cortex (vmPFC) (Milad and Quirk, 2002; Morgan et al, 1993; Quirk et al, 2000, 2003, 2006) in rodents. Functional neuroimaging studies of healthy humans have reported vmPFC activation during extinction (Barrett and Armony, 2009; Gottfried and Dolan, 2004; Kalisch et al, 2006; Milad et al, 2007b) and the later recall of extinction (Milad et al, 2007b; Phelps et al, 2004). Skin conductance measures of extinction memory are positively correlated with vmPFC activation (Milad et al, 2007b; Phelps et al, 2004) and vmPFC cortical thickness (Milad et al, 2005). Activation of the amygdala and insular cortex also may occur during extinction learning or recall (Gottfried and Dolan, 2004; LaBar et al, 1998; Milad et al, 2007b; Phelps et al, 2004), and greater amygdala responses during extinction have been associated with higher trait anxiety (Barrett and Armony, 2009). Finally, extinction can be modulated by context (ie, the surroundings in which extinction takes place), and the hippocampus has a role in this process. In rodents, dorsal hippocampal lesions reduce the context-dependence of extinction (Bouton et al, 2006). In a recent fMRI study, hippocampal activation to the CS+ occurred in the extinction context but not in the conditioning context (Kalisch et al, 2006). Hippocampal activation was also positively correlated with vmPFC activation in this study (Kalisch et al, 2006), suggesting that hippocampal-vmPFC interactions may be important for the contextual modulation of extinction.
Another way to examine the mediating functional neuroanatomy of fear or anxiety is to use specific pharmacological agents to provoke such states in healthy individuals during PET or fMRI scanning. For example, cholecystokinin-4 (CCK-4) is associated with increases in subjective states of fear and anxiety, as well as increased activation in the amygdala, insular cortex, claustrum, cerebellum, brain stem, and the ACC (Benkelfat et al, 1995; Eser et al, 2009; Javanmard et al, 1999; Schunck et al, 2006). In addition, two studies reported dACC increases during anticipatory anxiety preceding the CCK administration (Eser et al, 2009; Javanmard et al, 1999). It is important to keep in mind, however, that CCK-B receptor agonists like pentagastrin also have direct effects on stress axis stimulation independent of their effects on subjective experience of distress/fear (Abelson et al, 2005, 2008). Procaine administration has been associated with elevated subjective ratings of fear/anxiety, activation of the amygdala, ACC, and insular cortex (Ketter et al, 1996; Servan-Schreiber et al, 1998), and deactivation of neocortical structures (Servan-Schreiber et al, 1998). Furthermore, amygdala activity was positively correlated with subjective reports of anxiety (Ketter et al, 1996; Servan-Schreiber et al, 1998). Interestingly, those subjects who did not have a panic attack in response to procaine had greater activation in the rACC compared with those who did have a panic attack (Servan-Schreiber et al, 1998), consistent with the idea that the rACC may perform a regulatory or inhibitory function (Mayberg, 1997). The alpha-2 adrenergic antagonist yohimbine has likewise been associated with increased normalized blood flow in medial prefrontal cortex, insular cortex, and cerebellum in healthy individuals (Cameron et al, 2000). A major caveat in the interpretation of pharmacological challenge studies, however, is the difficulty in disentangling the effects that are specific to fear induction from the direct effect of a pharmacological agent on regional brain activity and from the non-specific effects of the pharmacological agent.
Over the past two decades, functional neuroimaging studies have shown that a core set of brain regions mediate responses to emotional stimuli in healthy humans. (For reviews, see Phan et al, 2002; Phan et al, 2004b). The relevance of these studies to fear/anxiety circuitry is two-fold: (1) A significant number of these emotional activation paradigms utilize stimuli that depict and/or elicit fear, and (2) these studies shed light on more general emotion-generating neurocircuitry. PET and fMRI studies have reported amygdala activation in response to emotionally negative photographs (Britton et al, 2006; Hariri et al, 2002; Irwin et al, 1996; Lane et al, 1997a; Paradiso et al, 1999; Phan et al, 2003b; Reiman et al, 1997; Taylor et al, 1998), odors (Zald and Pardo, 1997) and tastes (Zald et al, 1998). Several studies have reported amygdala activation to positive stimuli as well (Garavan et al, 2001; Hamann and Mao, 2002; Hamann et al, 1999, 2002; Liberzon et al, 2003), which suggests that the amygdala responds more broadly to emotionally arousing and/or salient stimuli (Phan et al, 2004b). Reappraisal of emotionally negative photographs is associated with reduced amygdala activation (Ochsner et al, 2002) and increased ventromedial prefrontal cortex activation (Urry et al, 2006). Finally, amygdala activation during encoding of emotionally arousing stimuli is correlated with the subsequent recollection of those stimuli (Cahill et al, 1996; Dolcos et al, 2004, 2005; Hamann et al, 1999).
Medial prefrontal cortex, including the rACC, also activates in response to emotional pictures (Lane et al, 1997a,b; Phan et al, 2003a,b, 2004a; Reiman et al, 1997) and may mediate self-referential processing (Kelley et al, 2002; Lane et al, 1997a; Zysset et al, 2002). Although the medial prefrontal cortex may activate regardless of task or valence, the rACC may be more likely to activate when a cognitive task is performed during scanning (Phan et al, 2002). Ventromedial PFC responses to fear-related images have been negatively associated with cortisol reactivity (Root et al, 2009). The dACC also activates in response to emotional photographs (Britton et al, 2006; Teasdale et al, 1999) and aversive tastes (Zald et al, 1998). Finally, the insular cortex is responsive to aversive stimuli (Phan et al, 2004a), internally generated sadness (Lane et al, 1997b; Reiman et al, 1997) and disgust-related stimuli (Britton et al, 2006).
Interestingly, the same neurocircuitry that has been implicated in fear/anxiety responses in humans is readily activated by stimuli that are not intrinsically threatening, but may convey information regarding the presence of threat in the environment or about the fearful emotional state of others. Responses in the amygdala are readily elicited by photographs of facial expressions, especially those of fear (Breiter et al, 1996a; Davis and Whalen, 2001; Fitzgerald et al, 2006; Morris et al, 1996; Vuilleumier and Pourtois, 2007; Whalen et al, 2001), even when presented below conscious awareness (Morris et al, 1998; Whalen et al, 1998, 2004). Emotional facial expressions have also been associated with activation in the dACC, rACC, medial frontal gyrus, and insular cortex (Fitzgerald et al, 2006; Gorno-Tempini et al, 2001; Morris et al, 1996; Phillips et al, 1997, 2004; Sabatini et al, 2009; Sprengelmeyer et al, 1998).
Brain responses to the relatively ambiguous facial expression of surprise have been shown, in some studies, to depend on the extent to which individual subjects interpreted these expressions as positive or negative; more negative interpretations were associated with greater amygdala and lower ventral medial prefrontal cortex activation (Kim et al, 2003). These findings are consistent with the notion that the amygdala and medial prefrontal cortex are reciprocally modulated (eg, Garcia et al, 1999). Furthermore, the experimental manipulation of the context in which surprise facial expressions are presented alters brain activation patterns in a similar way: surprise expressions associated with a negative context elicited more amygdala activation than those associated with a positive context (Kim et al, 2004). These amygdala activations were positively correlated with activation in the dACC (Kim et al, 2004).
Of relevance to our later discussion of anxiety disorders are findings that suggest that healthy individuals with high scores on anxiety measures have greater amygdala and insular cortex responses to emotional (angry, fearful, and happy) faces and less rACC activation than participants with normative scores on these measures (Bishop et al, 2004a,b; Stein et al, 2007). Similarly, trait anxiety has been positively correlated with amygdala responses to neutral faces (Somerville et al, 2004).
Studies of fear conditioning, pharmacologically induced fear, and responses to emotional stimuli and facial expressions have provided evidence that the human amygdala, although responsive to multiple salient stimuli, responds reliably and potentially preferably to stimuli that predict threat and can be involved in mediating fear/anxiety states. Given that patients with anxiety disorders experience fear and distress in response to possible predictors of threat, the amygdala has been hypothesized to be hyperresponsive in some anxiety disorders. In the next section, we will review the evidence related to this hypothesis.
Studies of extinction have highlighted the potential involvement of the vmPFC and hippocampus in the process of learning and remembering that stimuli that used to predict threat no longer do. One possible reason for exaggerated fear, anxiety, and distress in patients with anxiety disorders is that these emotional responses fail to extinguish or that extinction learning is not recalled even when specific cues no longer predict threat. Indeed, some studies have reported impaired extinction in several anxiety disorders, such as PTSD (Blechert et al, 2007; Milad et al, 2008; Orr et al, 2000; Peri et al, 2000; Wessa and Flor, 2007). Thus, the vmPFC and hippocampus are clear regions of interest in functional neuroimaging studies of anxiety disorders.
Finally, both the animal literature and studies reviewed above suggest that the dACC (and its likely homolog prelimbic cortex) and insular cortex respond to emotional stimuli or those that predict threat. As with the amygdala, hippocampus, and vmPFC, these regions are involved in multiple other functions; however, they might also have important roles in specific aspects of anxiety. For example, the insular cortex is thought to mediate the monitoring of internal body states, and has been found to be hyperresponsive in anxiety-prone individuals (Paulus and Stein, 2006). In summary, research on healthy individuals has suggested that all of these brain regions are prime candidates to examine in patients with anxiety disorders.
An important and often overlooked aspect of the fear/anxiety neurocircuitry is its overlap and interaction with the neurocircuitry that orchestrates the stress response. It is important to note that the concept of 'stress' used here is relatively specific. It does not encompass general concepts of 'subjective distress' or 'performance load.' Although these are useful concepts, they are heterogeneous by nature and are not likely to be associated with a specific neurocircuitry. On the other hand, the concept of a stress system that leads to activation of limbic-hypothalamopituitary-adrenal axis (LHPA) and secretion of stress hormones like corticotropin-releasing hormone (CRH), adrenocorticotropic hormone, and cortisol is quite specific and is likely to be highly relevant to the neurocircuitry of fear and anxiety. The neurocircuitry governing LHPA activation has been the focus of intense studies in rodents, primates, and humans because it has been repeatedly linked to the neurobiology of mood disorders (which is addressed in detail elsewhere in this volume), but the evidence linking LHPA axis abnormalities to anxiety disorders has been less consistent, sometimes confusing, and often oversimplified. At the same time, some of the same brain regions are implicated in both anxiety and stress responses, suggesting that these responses are interrelated and can influence each other. Furthermore, anxiety and mood disorders are highly comorbid, suggesting that some common abnormalities in neurocircuitry might be present in both disorders. In the following few paragraphs, we briefly address only the structural overlap in neurocircuits and the effects of stress system activation (or stress hormones) on anxiety/fear neurocircuitry.
Epidemiologically, major depression is highly comorbid with anxiety disorders like PTSD, panic disorder, and social phobia (Reiger et al, 1990), and anxiety symptoms are highly prevalent in depression (Frances et al, 1990). Furthermore, major subcortical components of the LHPA axis (eg, hypothalamus, hippocampus, amygdala, and BNST) have also been identified as key components of anxiety/fear neurocircuitry (albeit sometimes involving different subnuclei, for example paraventricular nuclei vs ventromedial hypothalamus for LHPA and fear neurocircuitry, respectively). More recently with the introduction of in vivo imaging methodologies in LHPA/stress research, the role of cortical structures like the insula and dorsal mPFC in the activation and inhibition of stress response, respectively, has been reported (Liberzon and Martis, 2006) as well as the role of subgenual ACC in self-induced sadness and depression (Mayberg et al, 1999). Together, these findings suggest a significant overlap in structures involved in the stress response and those involved in fear/anxiety responses (eg medial prefrontal cortex, insula, amygdala, hippocampus, and BNST). Finally, with respect to neurotransmitters involved, CRH is likely involved in the orchestration of both LHPA axis activity and many anxiety/fear responses. (For a review see Heim and Nemeroff, 2001.)
The activation of these overlapping regions in functional neuroimaging studies does not necessarily signify, however, activation of both the fear/anxiety response and the LHPA axis. As a matter of fact, activation of fear/anxiety does not necessarily activate an LHPA stress response, even in highly fearful (phobic) individuals (Curtis et al, 1976). In turn, activation of LHPA axis is not necessarily experienced subjectively as fear or anxiety. For example, morning awakening, food intake, and nausea all lead to LHPA axis activation without notable increases in subjective sense of fear. It is becoming increasingly clear that specific characteristics of experience (novelty, control, social support, etc.) are more salient for LHPA axis activation than degree of subjective distress or fear (Abelson et al, 2007). These facts help to better understand the findings of non-specific, or even sometimes counterintuitive, findings regarding the LHPA and stress responses in anxiety disorders such as panic disorder (Abelson et al, 2007) and PTSD (Yehuda, 2006; Yehuda et al, 1991). This also suggests that activation in specific cortical regions like mPFC or insula cannot be readily interpreted as a component of the fear response, and has to be considered within a context of a specific experiment, subjective report, symptoms, neuroendocrine profile, etc.
With these caveats in mind, important findings about stress exposure and LHPA axis activation affecting fear/anxiety responses have been accumulating. These can be seen in two general categories: (1) the immediate effects of stress or of stress hormones on fear/anxiety responses (eg, stress or stress hormone exposure immediately precedes, or is present during the fear/anxiety responses), and (2) delayed or developmental effects, (eg, stress exposure during developmentally sensitive periods, like early childhood, modulates fear/anxiety responses later in life). In the former category, it has been reported that exposure to acute stress in healthy individuals potentiates the anxiety response (Grillon et al, 2007). In addition, stress exposure (Trier Social Stress Test) led to enhanced galvanic skin responses to conditioned stimuli (CS+) during fear conditioning (Jackson et al, 2006). Interestingly, stress modulates fear responses differentially in men and women. Differential effects of stress on fear/anxiety in females vs males also have been demonstrated in animal studies. Chronic stress exposure led to impaired extinction recall of fear conditioning in male but not female rats (Baran et al, 2009). Stress exposure in animal studies also led to enhancement in contextual fear conditioning (Cordero et al, 2003). The effects of stress hormone exposure are somewhat more difficult to interpret because higher endogenous cortisol levels were associated with higher skin conductance responses (SCR) (Jackson et al, 2006), whereas administration of exogenous cortisol led to decreased SCR (Stark et al, 2006).
With respect to delayed effects of stress during the vulnerable developmental period, the findings are somewhat complex. Studies of early maternal separation in rodents (Plotsky and Meaney, 1993) and variable foraging in primates (Coplan et al, 1996) have revealed long-term alteration in stress axis responses and key neurotransmitter systems (for review see Heim and Nemeroff, 2001). In addition, recent findings of gene-by-environment interactions in PTSD (Binder et al, 2008) also point toward the possibility that early childhood experience might modify fear/anxiety neurocircuitry and contribute to the development of anxiety disorders. Direct evidence of these effects on fear/anxiety behavior is less convincing, however, as maternal separation in rat pups, which did alter relevant neurotransmitter systems, did not result in significantly enhanced startle response or decreased open field exploration as compared with non-separated animals (Caldji et al, 2000). Similarly, mixed results have been obtained in other studies where rats exposed to severe sporadic stress spent more time in open arms of an elevated plus maze but displayed increases in defensive probe burying behavior. Furthermore, animals exposed to milder chronic stress showed opposite changes (Pohl et al, 2007).
The character of the stress exposure (mild vs severe, prolonged vs short, predictable vs non-predictable) and the sex of the individual emerge as important variables that can define the long-term effects of stress exposure, but more experimental data are clearly needed. Similarly, little is known about the specific mechanisms by which stress exposure modulates fear/anxiety circuitry. It has been suggested, as stated above, that early developmental stress exposure alte


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really!!! we never noticed
Power outage in Superdome causes delay during Super Bowl XLVII
NEW ORLEANS — The electric Baltimore Ravens were apparently too high-powered for the Superdome. With Baltimore leading Super Bowl XLVII 28-6 early in the third quarter, the power kicked off inside the stadium, sending the game into a delay that lasted about 34 minutes.
It was a surreal sight for those inside the Superdome and those watching on TV. Slightly more than a minute after Jacoby Jones ran back an incredible 108-yard kickoff return to open the second half, with the 49ers facing 3rd-and-13 after an Arthur Jones sack of Colin Kaepernick, most of the lights in the stadium went out. Everything on the 49ers' side of the field — including the press box — went dark, as did all of the stadium's scoreboards.
Check out the video of [si_launchNFLPopup video='3f1be0a3fdb64911aba318df50f2e2c9']the power going out[/si_launchNFLPopup]. A GIF of it, via Deadspin:
Phil Simms, in mid-sentence on the CBS broadcast at the time, had his mic cut out, and for a long time during the delay the network had to use Steve Tasker and Jim Brown — who somehow had power on the field — to relay information to viewers. According to various reports, the flashy halftime show, performed by Beyonce, had an impact in the outage.
The NFL issued a statement saying, "Stadium authorities are investigating the cause of the power outage. We will have more information as it becomes available." But Entergy, which supplies power to the Superdome, tweeted to say, "Power issue at the Super Dome appears to be in the customer's side. Entergy is providing power to the Dome. At all times, our distribution & transmission feeders were serving Superdome. We continue working w/ Superdome to address any issues."
Long after the game had ended, Entergy and SMG (the Superdome's management company) issued a joint statement explaining that "a piece of equipment that is designed to monitor electrical load sensed an abnormality in the system. Once the issue was detected, the sensing equipment operated as designed and opened a breaker, causing power to be partially cut to the Superdome in order to isolate the issue.
"Backup generators kicked in immediately as designed. Entergy and SMG subsequently coordinated start-up procedures, ensuring that full power was safely restored to the Superdome."
New Orleans mayor Mitch Landrieu calledit "an unfortunate moment in what has been an otherwise shining Super Bowl week for the city of New Orleans. In the coming days, I expect a full-action report from all parties involved.
To the sellout crowd's credit, the atmosphere remained subdued despite the somewhat unsettling situation. The two fanbases traded "Let's Go Ravens" and "Let's Go Niners" cheers, with a wave mixed in as well.
PHOTOS: Best of the game | Beyonce's halftime show
An announcement was made over the stadium's public address system after several minutes, but the lack of power on the 49ers' side of the field also knocked out the speakers pointing that direction, meaning that a large chunk of the crowd was not privy to the message relayed.
VIDEO: Best & worst of Super Bowl XLVII commercials
The crowd began cheering wildly as the lights and scoreboards finally came back to life, coupled with multiple announcements that the game would resume shortly.
Twitter, naturally, had a field day with the fiasco, with a slew of jokes being hurled around during the delay. Below is a sampling of the best ones.
don't act like you've never blacked out in New Orleans.
— Abby (@abbytrott) February 4, 2013
Sean Payton is somehow going to get suspended again for this.
— Tom Mantzouranis (@themantz) February 4, 2013
Guaranteed that the NFL will give Ray Lewis a tackle credit for knocking the lights out.
— Matt Miller (@nfldraftscout) February 4, 2013
Oh, NOW someone gives a damn about the people without power in the Superdome!
— Michael Chaney (@mjchaney) February 4, 2013
This has been the worst second halftime in Super Bowl history.
— Rob Peterson (@ShotDrJr) February 4, 2013
— Joe Schmidt (@joeschmidt) February 4, 2013
— Ashley Burns (@MayorBurnsy) February 4, 2013
I say New Orleans just lost the right to host any future Super Bowls. Biggest US sporting event of the year....and that happens? Embarrassment. Nope, sorry...you're done.
On the flip side....why not have the Super Bowl in Hawaii every year? You get a truly neutral field with both teams having to travel, you get great weather....instead of a Pro Bowl maybe have a flag football charity game with all pros playing for a charity, and hold some of those good old skill contests in the run up to the Super Bowl.
How dare the football get in the way of the commercials and the latest greatest crap pop concert. Fact is when you get the majority of women involved in anything sporting (Olympics with gymnastics, synchronized swimming, etc) they just plain ruin the competition or at least the experience.
The NFL could not afford to have a blow out. Had to go to plan B to try SOMETHING to make sure the game is close just like they have for over a decade. The NFL - influencing the outcomes of football games since 2002.
Wasn't NO black enuf to begin with?
New Orleans - still a mess.
— Ashley Burns (@MayorBurnsy) February 4, 2013
Theres some unbiased news coverage of one of "the best" tweets.
They call this journalism?
Okay, we all know that the blackout wasn't a deliberate ploy by the NFC New Orleans Saints, to stem the Ravens overpowering momentum and let the NFC Forty Niners get back into the game, right? We all know that? Right? Because we don't believe in conspiracies. RIGHT?
@Rickapolis , right. Because that wouldn't even make sense. Why would the Saints give a rat's butt who won that game? This isn't college...there are no poll implications for next season or anything like that...

subset: commoncrawl


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Series 1 Episode 1
A female NYPD detective possesses the special ability to remember everything.
A female NYPD detective possesses the special ability to remember everything.
Carrie calls on her own childhood trauma to help her connect with a witness.
Carrie and Al uncover a series of interlocking blackmail schemes.
Carrie's extraordinary memory of a crime scene leads her to an upstate prison.
Al discovers that his old friend is being investigated by Internal Affairs.
Carrie is investigating an heiress' mysterious death.
Carrie's mother's memories bring her closer to identifying her sisters murderers
Carrie is lead into the middle of a deadly revenge plot.
Al and his team suspect the high school student was murdered.
A seventeen-year-old has been shot and killed.
Al and his team are summoned to a mental hospital.
A young ironworker is found murdered at a construction site.
Carrie is led to a fraternity party where drugs are used to undermine her memory
Carrie is alerted to an upcoming murder by a brash but anonymous killer.
Carrie goes undercover at a local marina.
A dead body mysteriously appears on a minor league baseball field.
Carrie and Roe kill David Jacobs after chasing him in a dark alley.
A nineteen-year-old is shot and killed as she's leaving a tennis training centre
Carrie's professional and personal lives become dangerously entangled.
Carrie and Al are in search of a mad bomber.
Carrie believes the serial killer who's been stalking her has been murdered.
The arrest of a murder suspect leads Carrie and Al to their hometown of Syracuse


text: Al Gustin's new book, "Farm Byline," is a good read and it might be a good Christmas gift for someone on your list. Gustin recently retired from a 45-year career as an ag journalist in North Dakota. The book is a collection of the columns he wrote for the North Dakota Association of Rural Electric Cooperatives between 1974 and today. The columns in the book I liked best were about his own life on the farm and the everyday life of North Dakota farmer and ranchers &ndash…Continue Reading


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Julia Ormondactress
Born: 1/4/1965
Birthplace: Surrey, England
In the United States, Ormond is known for her work in Smilla's Sense of Snow (1997), Sabrina (1995), Nostradamus (1994) and Legends of the Fall (1994). British audiences were introduced Ormond when she played a heroin addict on the British television series Traffik (1989). Ormond won the London Critics' Award for Best Newcomer in 1988 for her role in Faith, Hope and Charity. She graduated from the Webber-Douglas Academy of Dramatic Arts.
Information Please® Database, © 2007 Pearson Education, Inc. All rights reserved.
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NDSU Libraries Falls Open House
Submit Your Event | Questions? E-mail Us
The NDSU Libraries will be holding our annual Fall Open House on Wednesday, October 3rd and Thursday, October 4th from 11am-3pm at the Main Library. The two day event, held during Homecoming week, will include short story and poetry readings, demonstrations of databases, information on NDSU and local library resources, and door prizes from local businesses. Special presentations from NDSU alumni include Ankit Rauniyar's award winning vision of a new library building and Mitzi Brundale's talk on murder mysteries and writing will be featured. Thundar, NDSU's mascot, will make an appearance on Wednesday for a meet and greet. Refreshments will be provided.
Admission Information: Free
NDSU Main Library
Fargo, ND 58105
Events Search


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TALLAHASSEE -- Ethics reform is a frequently prescribed but seldom swallowed political tonic in Florida. Maybe that will change next year, but history and the alignment of politicians' incentives suggest otherwise.
Corruption and cries for reform have become a predictable two-step. When controversies erupt, policymakers advance tighter restrictions on their behavior or ability to extract benefits from the well-heeled interests cooing over them.
Now, incoming Senate President Don Gaetz, R-Niceville, says he wants to curb some of the abuses of recent years.
The last time lawmakers passed a wholesale ethics reform was 2005, when they banned lobbyist gifts to lawmakers. That push came after four industry-supportive GOP senators had taken a lobbyist-paid, $48,000 trip to a Magna Entertainment Corp. casino in Toronto.
But critics say that ban led lobbyists to instead pour cash into "Committees of Continuous Existence," which lawmakers can use to buy more lavish meals, trips and "party-building" high-living than they could get away with pre-reform.
Two weeks ago, former Sen. Mandy Dawson, D-Fort Lauderdale, began serving six months in federal prison for not paying taxes on under-the-table payments she got from South Florida lobbyist Alan Mendelsohn.
That influence-peddling scheme rattled Tallahassee, because Mendelsohn was a GOP fundraiser and political player through the Florida Medical Association. CCEs let the peddlers funnel the cash to lawmakers legally, although there are some restrictions on its use.
Gaetz – without naming names -- said he doesn't want legislators to "collect money into a CCE and then live off of it."
He also wants lawmakers to stop voting on bills when they have a conflict-of-interest -- and to declare those conflicts before a vote instead of 15 days afterward, as the law now requires.
In the December 2009 special session to authorize Central Florida's SunRail commuter train, Rep. Baxter Troutman, an heir to the Ben Hill Griffin Jr., agricultural empire, declared family business shareholders shouldn't vote because they had contracts with CSX Corp., the railroad selling the SunRail lines to the state. Those shareholders included Troutman's estranged cousin, Senate Budget Chairman J.D. Alexander, a prominent SunRail backer who got a legal opinion that he could vote for the bill.
Then there is the elephant in Gaetz's cross-hairs: Fellow Northwest Florida ex-lawmaker Ray Sansom, who resigned as House speaker in 2009 over shady appropriations he helped steer to a college that then hired him at a six-figure salary.
Gaetz wants to stop such "co-employment" situations, where legislators with access to public dollars get job offers from public agencies with need for those dollars.
"They somehow have this divinely inspired knowledge about education, and they get a job in public education. Shocking!" Gaetz said.
"It's what we in Okaloosa County call a walkin' around job."
Outgoing Senate President Mike Haridopolos, R-Merritt Island, was admonished last year by his chamber for failing to disclose a $400,000 investment home and other income. Afterward, he pushed an ethics bill to, among other things, ban lawmakers from taking side jobs in Florida's education system.
But, Sens. Steve Wise, R-Jacksonville, Evelyn Lynn, R-Ormond Beach, and Gary Siplin, D-Orlando, killed it, while lambasting the media and the lobbyist gift-ban.
Gaetz was a co-sponsor of last year's deep-sixed ethics bill, and his power ensures the idea will re-surface. But history suggests it must overcome well-fed politicians unwilling to stop the gravy train while they have a seat.
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Homepage > Fashion > Watches & Jewelry >
Barber Dime Pendant
American history meets contemporary fashion in our stunning Barber dime necklace. The .900 fine silver Liberty coin was minted from 1892 to 1916. And appears here mounted on a simple polished silvertone pendant, with both obverse and reverse displayed. A unique three-strand chain combining cable, bar and rope links add a special touch and is about 20 1/2" in length.
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How do you deal with that?
Try a contract. Contracts are part of adult life. Offers of employment, mortgages, rental agreements, car leases ... all are contracts. With that understanding, you can craft something mutually acceptable with your teen.
1.) Identify your issue: Spending money, use of car, social schedule, homework.
2.) Each party lists their responsibilities: "I will..." "I can provide..." It is best, where possible, to phrase these in positive terms.
3.) Brainstorm consequences of non-compliance. Again, this is not "treating him/her as a child." Most contracts have a penalty clause; many domestic contracts also include a dispute resolution section.
4.) Print two copies: One for the teen to keep, and one to be posted someplace central.
Tips for parents: Though you'll have an agenda for this document, you can't write it single-handed. Like any contract, it will be negotiated, Don't be too generous; if you make a concession, make sure your teen understands that you have done so. Don't make two in a row if your child hasn't made one yet! Concessions are traded -- no one gets everything they want, but, if everyone cooperates with the process, everyone gets most of it.
Welcome to the Adult World.
Mother of three (teens), step-mother of five (teens), home daycare operator of five (todders), and STILL SANE!! NOTHING is impossible...
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Solubility of elements is what affects the life of the membrane and how it can scale. Take a piece of marble and try to dissolve it in water. Do the same with salt. You will notice that the salt is highly soluble. It is this solubility that prevents it from scaling a membrane. It is much more complex than I described, but you get the point. http://www.lenntech.com/antiscalants.htm Here is an interesting sales pitch for anti scalants. Softening is not an economical method for treating larger RO systems. Smaller units are fine. For residential units, the membranes are considered diposable because the cost of treatment can greatly exceed the cost of the membranes.
As to the TDS of softenerd water, since it is an Ion Exchenge process, Softened water will usually have a higher TDS than unsoftened water and the handheald TDS meters are not designed for serious analytical testing, they are for information, comparisons, etc. It is what makes up the TDS that is the important factor. The sodium is much easier to deal with than the calcium and magnesium in the water since has nearly no scaling potential.


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HOME Indiana Hoosiers Gear Indiana Hoosiers Mens Indiana Hoosiers Mens T-Shirts Indiana Hoosiers Mens T-Shirts Short Sleeved (237 items) Product ID: 860993
Main Content
Order today, receive no later than
Order today, receive no later than
Tuesday, April 29th
Some limitations apply
Your Hoosiers pride is certainly something to brag about. Whether it's game day or nap time, you boast your IU spirit proudly. Throw on this comfy adidas The Balboa tri-blend tee to show off your Hoosiers pride wherever you go. This super soft tee features a huge Indiana wordmark logo in distressed screen print on the chest for the right touch of timeless IU spirit!
- 50% Polyester/37% Cotton/13% Rayon
- Screen print graphics
- Tagless collar
- Lightweight heathered tee
- Imported
- Officially licensed Hoosiers tee
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Manufacturer direct items are shipped directly from the manufacturer. These items are not available for international or expedited shipping.
Customized items can be personalized with options such as your name, your favorite number, and/or designs. Some options may be limited by league rules.


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Walter Kerr Theatre
219 West 48th Street
Between Broadway & 8th Avenue
New York NY 10036
View on map
Discount Tickets for Groups
Add to My Event List
A Gentleman's Guide To Love & Murder is "The new undisputed King of Musical Comedy!" (Time Out New York) This Broadway smash tells the uproarious story of Monty Navarro, a distant heir to a family fortune who sets out to speed up the line of succession using a great deal of charm… and a dash of murder. Tony® winner Jefferson Mays (I Am My Own Wife, Gore Vidal's The Best Man) gives "a performance that deserves to be immortalized in Broadway lore," (The New York Times) playing all eight doomed heirs who meet their ends in the most creative and side-splitting ways. He stars alongside the debonair Bryce Pinkham (Ghost, Bloody Bloody Andrew Jackson) as Broadway's homicidal hunk, Monty Navarro. Don't miss this drop-dead hilarious show that "Restores our faith in musical comedy!" (The Hollywood Reporter)
Lisa O'Hare, Lauren Worsham, Jane Carr, Pamela Bob, Joanna Glushak, Eddie Korbich, Jeff Kready, Mark Ledbetter, Jefferson Mays, Bryce Pinkham, Jennifer Smith, Don Stephenson, Price Waldman, Catherine Walker
Author: Robert L. FreedmanMusic: Steven LutvakLyrics: Robert L. Freedman & Steven LutvakDirector: Darko TresnjakChoreographer: Peggy HickeyProducer: Eight to Go LLCPress Agent: O&M Company
2 hours and 20 minutes, including intermission
View Full Calendar
$35.00 - $137.00 (Ticket prices include a $2.00 Facility Fee.)
See this week's prices
May be inappropriate for 10 and under.Children under the age of 4 are not permitted in the theatre.
Monday - Saturday: 10am - 8pmSunday: Noon - 6pm
A Gentleman's Guide to Love and Murder
Telecharge Mail OrderP. O. Box 998 Times Square Station New York, NY 10108-0998
None available, however large bags may be checked by inquiring at the theatre.


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Send a link to this page to your friends and colleagues.
The short-term legislation enacted to avoid the "fiscal cliff" at the start of 2013 has long-term consequences for Medicare beneficiaries' access to diabetes testing supplies (DTS). The legislation drastically cuts independent community pharmacy reimbursement for DTS and will likely decrease beneficiary access. Decreased beneficiary access to DTS could result in less patient adherence and increased long-term costs due to avoidable complications in the management of diabetes.
The National Community Pharmacists Association has repeatedly outlined the shortcomings in such an approach. Round 1 of the competitive bid program has validated NCPA's concerns, including identifying rampant waste in mail order and the strong patient preference for a face-to-face health care experience with local health care providers such as independent community pharmacists.
The solution is simple. NCPA is asking the U.S. Congress to put a stop to these drastic cuts to reimbursement to independent community pharmacies for DST. These small businesses often are in underserved rural and inner-city locations, and preserving access to these essential medical products and the consultation on their proper use for some of the most vulnerable patients is a must.
A number of reports have identified problems with the Competitive Bidding Program and the use of mail order. The Office of Inspector General of the U.S. Department of Health and Human Services conducted a study for officials at HHS' Centers for Medicare and Medicaid Services in 2012. They noticed a trend of seniors switching from mail order to non-mail providers, like community pharmacies, soon after Round 1 of CMS' competitive bidding program took effect in certain segments of the country.
According to OIG, the use of non-mail order DST increased by 33 percent, while mail order DST decreased by 71 percent. To figure out why patients switched away from mail, OIG interviewed beneficiaries. Ten percent of beneficiaries made the switch from mail due to either unsatisfactory service or because they were unsatisfied with mail. The remaining beneficiaries stated they switched because either their previous provider didn't win the competitive bid or didn't offer the product they used. Presumably most, if not all, of these seniors had the option to choose a mail order provider but decided against it.
The OIG report further validates concerns by NCPA member pharmacists and previous statements by CMS of witnessing mail order oversupplying and wasted health care dollars that can occur through "auto-shipping" of DTS. Five percent of beneficiaries received unsolicited DTS. Beneficiaries reported receiving an average of five unsolicited boxes of DTS.
NCPA also conducted a survey in 2012 of 400 community pharmacy owners where 92 percent of independent community pharmacies stated they would likely leave the Medicare Part B program and cease supplying DTS if forced to suffer a sharp reduction in reimbursements. Over 50 percent of community pharmacies said that the average Medicare diabetic patient comes to them at least three times per month for diabetic supplies and/or counseling. In addition, 83 percent of community pharmacists said that the impact on patients if they had to obtain diabetes supplies from mail order would be significant; and 45 percent of community pharmacies deliver diabetes testing supplies to assisted living facilities.
In addition to these drastic cuts, due to changes in definitions of "mail order" and "non-mail order," CMS will prohibit independent community pharmacists from delivering DTS to homebound beneficiaries and assisted living facilities beginning July 1, 2013. The ban was included in CMS' competitive bidding policy for DTS. NCPA encourages Congress to address CMS' oversight and ensure some of the frailest Medicare beneficiaries are not faced with the harsh reality of having no other way to receive the supplies they need to stay alive.
Categories: Medicaid, Blood Sugar, Diabetes, Diabetes Health, Diabetes Health Magazine, Diabetic
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Wilton® Bee Mine Candy Heart
These sweet treats are fun to make and give to your sweetheart on Valentine's Day.
Designed by Wilton
Material List
- Wilton Cookie Sheet
- Wilton Heart Comfort Grip Cookie Cutter
- Wilton Valentine Candy Making Mega Pack (Butterfly mold used)
- Wilton Tip, 3
- Wilton Candy Melts (White, Pink, Red, Light Cocoa)
- Wilton Sweetheart Sprinkle Mix
Project Instructions
Place Heart Comfort Grip Cookie Cutter on Cookie Sheet and fill with melted light cocoa candy; refrigerate to set and unmold.
Mold butterfly using instructions in candy mega pack; refrigerate to set.
Attach white jimmies from heart mix to form dotted line on candy heart.
Use melted candy in cut parchment bag to print "LOVE BUG".
Attach two red hearts from heart mix to candy with melted candy.
Attach butterfly with melted candy; refrigerate to set.


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Got a question? Something on your mind? Talk to your community, directly.
by Barbara Linert
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by MRI School of Minnesota
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How Technology Is Making It Great To Be A Music Fan
Music brings people together, but technology is strengthening those connections.
Music brings people together, but technology is strengthening those connections.
Google Play Music is now the first outside app that can control Sonos' smart home speakers.
At $35, the Chromecast is a marvel. But how well does it hold up for home audio?
Twitter and Billboard will now collect and show off the most popular music conversation on the social network.
We spent some time with the reinvented Sonos app—which may be the key to the modular speaker-maker's survival.
What do you get when you cross a Chromecast with a Sonos? A less expensive way to stream music across your house.
Beats Music feels like it was designed by someone who wears cool shoes and doesn't talk about algorithms.
Dr. Dre's new streaming music service looks to have learned from the mistakes of Spotify, Pandora et al.
Giving out freebies Oprah-style may not be enough to keep the streaming-music service afloat.
The hills are alive ... with the sound of technology!
From audiophile to casual music listener, we've got great-value picks for every budget.
Spotify is giving users free access on smartphones, but only if you hit "shuffle."
Google Glass wants to be a viable iPod alternative. It's not there yet.
The streaming era is the next music industry ice age.
Finally we know how much musicians make per stream—and boy, is it not much.
Glass is not just about seeing, it's now about listening, too.
The popular music app now supports Google's Chromecast TV dongle, bringing the grand total of third-party streaming sources to three.
With its new YouTube award show, Google proves that it's painfully hip—and poised to own social TV from every angle.
These off-the-beaten-track music services offer innovative features you're not going to find on Spotify, iTunes or Pandora.
The what's-that-song app now identifies music and TV shows automatically.
With the launch of All Access, Google joins the streaming music business. Why the giant could disrupt the space dominated by Spotify and…
According to published reports, Google has already struck licensing deals with the three largest music companies.
Spotify and Rdio are the best music subscription services in the U.S., but neither is perfect. Here's what the ultimate streaming service…
Twitter's new music app is here. Artists should love it, but fans aren't going to find as much to like.


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Get on your bike this holiday
- 16 July 2012 15:30
- Posted by Chris Eccles
Love City? Love cycling? Then here's a wheely good piece of news to ring your bell!
The ever-popular British Cycling Summer School is returning to the Etihad Stadium with a 3-day cycling course.
We are giving children under 16 the opportunity to improve their cycling skills and build their confidence to ride safely on today's challenging roads.
The course costs £25 for two days of Go-Ride coaching from experts at British Cycling Cycle Training followed by one day of Bikeability training to help you cycle safely on the roads with confidence. You also get a peek behind the scenes at the Etihad Stadium
If that is not enough we are also throwing in a High Viz Vest, British Cycling Bag, British Cycling Water Bottle.
The course will run 23, 24, and 25 July from 10am-3pm each day with registration on day one taking place at 09.50. Children will need to bring their own bike, helmet and a packed lunch.
Each child will require a completed parental consent form and in order to secure your place you will need to contact the team on 0161 274 2129 or firstname.lastname@example.com.


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As we celebrate the first UN Sport for Development and Peace Day, we also celebrate ASOP, a program dedicated to using sport as a tool to deliver community outcomes.
ASC CEO Hollingsworth congratulated the Bingham Cup Sydney 2014 organising committee on finalising a draft anti-homophobia framework for the ARU, NRL, AFL, FFA and Cricket Australia.
Fresh off a record-equalling seventh national 400-metre hurdles title, we spoke to Lauren Wells about her quest for more 'bling' in 2014.
AIS Sports Tally signals upward trajectory for Australia's international sporting success
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Plus Size Solid Tank
$18.50buy one, get one 50% off
Whether under a jacket, layered with a sweater or on its own in warmer weather, this tank is a year-round staple. Imported.
- Scoop neckline
- Stretch fabric
- 95% polyester/5% spandex
- Machine Wash
- sku #:
Available Colors
Complete the Look
Plus Size Solid Tank 16 16
Take out the tag! The top itself fits well and is comfortable, BUT the tag is sewn in using invisible nylon thread. When I first put it on, it felt like a fire ant stinging my neck. I tried trimming the thread, but no luck. I had to take a seam ripper and remove the tag. I ended up with a tiny hole in the blouse where I removed the tag. It's a small price to pay, though, to not have to live with the agony of those tiny plastic threads torturing me. April 15, 2014
Nice layering piece Too thin to wear alone, but nice and comfy under a jacket. A little long, but not a problem when tucked in. April 6, 2014
Too tight The tank fit nicely through the bust but was too small in the waist. March 28, 2014
All my other tops are 1X and they fit and look good, but this top was way to snug... February 12, 2014


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Peter Rabbit™ Garland
No longer available
- Overview
Dress up your home for Easter with our Peter Rabbit Garland. Five flags printed with vibrant scenes from The Tale of Peter Rabbit are joined by a string of beads and colorful eggs.
- 60.5" long x 6" high
- Five cardboard flags are illustrated with Beatrix Potter scenes.
- The garland is decorated with painted Easter eggs and wooden beads.
- Dimensions & Care
- Overall: 60.5" long x 6" high
- Flag (5): 4.5" wide, 6" high
- Dust with a soft, dry cloth.
- Shipping Info
Please allow 5-7 business days for delivery. Delivery estimate includes monogrammed and gift-wrapped items.
Easter is April 20th. Order by 4/15, 11PM PT for monogram shipping. Order by 4/16, 9AM for standard shipping.


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U.S. Under-17 WNT Arrive in New Zealand for World Cup
Oct 26, 2008
GROUP C SCHEDULE: The USA was drawn into Group C at the U-17 Women's World Cup and will face three different styles of play in Japan, Paraguay and France. This current group of U-17 players have never faced any of their first round opponents but surely the Japanese, who lost to North Korea in the championship game of their qualifying tournament, first-time FIFA women's world championship participant Paraguay and rising youth women's power France will all present unique tests for the young Americans. Each team will play three group matches in seven days. The USA will have the advantage of a short bus ride to Auckland for its final group game, while the other two Group C teams will fly down to Christchurch on the South Island for their third match.
2008 U-17 Women's World Cup Group C Schedule
Date Match Venue Local Time / ET
Oct. 30 Japan vs. USA Waikato Stadium (Hamilton) Noon / 7p.m.
Oct. 30 France vs. Paraguay Waikato Stadium (Hamilton) 3 p.m. / 10 p.m.
Nov. 2 Paraguay vs. USA Waikato Stadium (Hamilton) 1 p.m. / 8 p.m.
Nov. 2 Japan vs. France Waikato Stadium (Hamilton) 4 p.m. / 11 p.m.
Nov. 5 Paraguay vs. Japan QEII Park (Christchurch) 4 p.m. / 10 p.m.
Nov. 5 USA vs. France North Harbour Stadium (Auckland) 4 p.m. / 10 p.m.
U17 WNT ON MT: Fans can follow all the U.S. U-17 matches as they happen live on ussoccer.com's MatchTracker. With the time difference in New Zealand, the matches for the most part take place during some prime viewing time, early evening on the East Coast, which means you might have to DVR Ugly Betty, Extreme Home Makeover or Criminal Minds, but it'll be worth it.
LIVING HISTORY: The 21 players on the U.S. Under-17 Women's National Team roster are making history as the first-ever Americans to compete in a U-17 Women's World Cup. FIFA, the world governing body of soccer, has held two U-19 Women's World Cup and one U-20 Women's World Cup, but this tournament will mark the first world championship for this age group, tagging these young players as pioneers of sorts before any has hit her 18th birthday. In 1991, another group of young U.S. players made history by winning the first-ever FIFA Women's World Cup. Some symbolism that should not be overlooked: That historic triumph was 17 years ago and 16 players on the U.S. roster were born in 1991. Fourteen of those were born less than a year earlier when U.S. captain April Heinrichs lifted the World Cup trophy after the U.S. defeated Norway in the Women's World Cup Final on Nov. 30, 1991. Three days later, U.S. U-17 midfielder Kate Bennett was born. Three days after that, U.S. defender Alexis Harris was born. Hopefully, none of this makes U.S. assistant coach Amy Griffin (who was on that 1991 Women's World Cup squad) feel old. Stay tuned to usssoccer.com later in the tournament to read more from Griffin (who won the World Cup title as Amy Allmann) about her first World Cup experience.
USA WILL WATCH BEFORE IT PLAYS: By the time the USA kicks off its first match on Oct. 30 against Japan, the players will be more than ready to play as four matches will have already been completed. The tournament kicks off with a one-off Group A contest between host New Zealand and Canada on Oct. 28 and continues with three more games on Oct. 29, including the other game in Group A (Denmark vs. Colombia) and the first matches in Group B (Costa Rica vs. Germany and North Korea vs. Ghana). You may recall that Germany kicked off the 2002 FIFA Men's World Cup against Costa Rica, a 4-2 German win. The U-17 women will surely be looking to at least equal the goal output from the historic 2002 FIFA World Cup opener.
LAST TIME IN NZ: The U.S. U-17s started 2008 where it hopes to end it – Auckland, New Zealand – the venue for the USA's first three games of the year as well as the 2008 FIFA U-17 Women's World Cup championship game. Last January at the Future Stars Tournament, the USA defeated Australia (6-0), New Zealand (5-0) and Germany (3-2) to win the tournament and kick-start a year in which the team has compiled a 16-1-1 overall record. The Mewis sisters – Kristie and Samantha – led the team in that tournament, combining to score seven of the USA's 14 goals. Kristie Mewis scored twice in the win over Germany. Courtney Verloo scored twice in the tournament as did Tani Costa, who will miss the U-17 World Cup due to injury.
COSTA OUT, BROCK IN: The U.S. team suffered a blow even before it got onto the plane for New Zealand as forward Tani Costa was ruled out of the tournament about 36 hours before the USA departed due to due an ankle injury. The Hawaiian hurt her right ankle during the most recent training camp and the injury was deemed serious enough to preclude her from World Cup action. Costa has been a regular player in the U.S. pool this year. She has scored five goals in five international matches during 2008, including two goals in the championship game of CONCACAF Qualifying last July. Costa will be replaced by Hayley Brock, a 5-foot-9 forward out of Acton, Mass. The speedy Brock is uncapped at the U-17 level.
U.S. Under-17 Women's National Team
2008 FIFA U-17 Women's World Cup Roster
GOALKEEPERS (3): Alexa Gaul (Naperville, Ill.), Jennifer Pettigrew (Kearney, N.J.), Taylor Vancil (South Elgin, Ill.)
DEFENDERS (6): Amber Brooks (New Hope, Pa.), Cloee Colohan (West Point, Utah), Crystal Dunn (Rockville Center, N.Y.), Alexis Harris (Plano, Texas), Rachel Quon (Lake Forrest, Ill.), Julia Roberts (Fredrick, Md.)
MIDFIELDERS (8): Kate Bennett (Clyde Hill, Wash.), Morgan Brian (St. Simons Island, Ga.), Elizabeth Eddy (Costa Mesa, Calif.), Olivia Klei (Pleasanton, Calif.), Mandy Laddish (Lee's Summit, Mo.), Kristie Mewis (Hanson, Mass.), Samantha Mewis (Hanson, Mass.), Erika Tymrak (Bradenton, Fla.)
FORWARDS (4): Hayley Brock (Acton, Mass.), Vicki DiMartino (Massapequa, N.Y.), Samantha Johnson (Palmdale, Calif.), Courtney Verloo (Tualatin, Ore.)
STATE OF THE GAME: Fourteen states placed players on the 2008 U.S. Under-17 Women's World Cup Team and not surprisingly, California was tied for most at three. But give Illinois and Massachusetts credit for also having three players on the roster. Combine New York and New Jersey and that's three more players, but with the West (Utah, Oregon and Washington), the South (Texas, Florida and Georgia), the Midwest (Missouri) and the East (Maryland and Pennsylvania), the young female soccer talent is clearly coming from all across the United States.
HELLO HAMILTON: The U.S. U-17s will spend 11 days in Hamilton, the seventh largest city in New Zealand with a population of around 131,000 people. While anywhere in New Zealand is pretty much near a coast, Hamilton is New Zealand's largest inland city. Still, there is plenty of water. The country's longest river – the Waikato – flows 10 miles through the center of the city including right past the USA's hotel, which is also hosting the other three teams in Group C.
SISTER ACT: The Mewis sisters – Kristie (17) and Samantha (16) – are the first-ever siblings to represent the U.S. Women's National Team at a world championship event at any level. Twins Ronnie and Lorrie Fair were the first sisters to play in the same game for the U.S. women when both saw action against England on May 9, 1997, in San Jose, Calif. Lorrie started and Ronnie came off the bench. They would play one more match together, that coming two days later against England in Portland, Ore. Ronnie earned three WNT caps during her career, Lorrie earned 120, including appearances in the 1999 Women's World Cup (where she was the youngest player on the roster) and the 2000 Olympics.
Stat of Note
Sixteen different players have scored for the U.S. U-17s in official matches this year. Thirteen of them are on the Women's World Cup squad, not including Tani Costa, who was initially named to the team before bowing out with an ankle injury.
News Feb 5, 2014


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Every season for the last six years, Covenant senior Richard Coppola has played a sport at for the Eagles. Since seventh grade, he's been a member of the school's football, swimming and baseball teams. Now, in his 18th consecutive season, Coppola is more valuable to his team than ever.
For Coppola, the more sports he played, the better he did in school. After 18 straight seasons, he is now a member of Covenant's high honor roll.
"I never planned to do three sports every year since 7th grade, but I operate better when I'm busy," he said.
"I'm just impressed with that, that each season that comes around he just gets out those clothes and gets ready to go, and he just devotes himself to it," said Covenant baseball coach Doug Smethurst. "I've just been very impressed with his dedication."
Now in his final season, Coppola is captain of his baseball team and he's also the Eagle's ace and best hitter.
"As Richard goes, so goes our team," says Smethurst. "If he's hitting the ball well it really is a huge plus for our team, we tend to get momentum from that. If he's throwing the ball well on the mound, we just kind of fall right in line and it ends up being a pretty good day for us."
Coppola plays football and is an all-VIC swimmer, but he says the baseball diamond is his favorite place to be.
"Every other sport is almost purely physical, and baseball, you could be the greatest athlete in the world and still not be very good at baseball because you have to think through so many things, you have to be quick on your feet, not just physically but you have to know what to do at all times. It's a challenge."
When he's not focused on sports or school, Coppola is involved with his church, where he has led retreats for the last two years.
"I like being able to help kids kind of figure things out for their own, and just being able to, if they have any questions about the retreat or about anything bigger than that, I like to be able to help them out with that and kind of being a mentor to them."
He says those experiences planning and leading retreats have helped him become a better leader on his baseball team.
"It's kind of similar to the retreat in that younger kids, because we're a very young team, younger kids come up to you and ask you about situations, or they're just upset with something, they're not playing well and they're not happy about that, that you can be there for them."
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|Running Touch - Player Release in Crosshairs
|RUGBYmag Premier - Columns and Opinions
In the statement, the IRB said: "Player release is central to the integrity and economic sustainability of the international Game and the IRB continues to be proactively committed to assisting Unions with player release issues when requested by them to do so under Regulation 9.
The Regulation is designed to deliver a fair, equitable and proportionate framework for facilitating the release of the world's best players for international duty within designated windows without impediment irrespective of country of employment. This Regulation goes to the very core of supporting the integrity of the international Game.
The IRB takes any breach of the Regulation very seriously and acts on release issues where it is formally requested to do so by a Union or if it is presented with credible evidence provided by a Union or recognised Rugby body that would allow it to pursue its own enquiry. In respect of the former, the IRB has collaborated with Unions over a long period to successfully facilitate the release of players for international duty and will continue to do so.
Unions also have a clear obligation to do everything possible to uphold the Regulation within their territory or they risk significant sanctions.
The IRB is currently monitoring player release issues during the November 2012 window and the matter will be the subject of discussion at the IRB November 2012 meetings in Dublin."
Sometimes clubs get around all the player release issue by persuading a player to retire from international rugby, which, said Melville, "is not something we want."
In the end, because the professional rugby season is so long, and has to be because clubs don't make massive profits on games and therefore need to play 40 or more games to make it all pay, clubs often have to play during international windows.
"In short, Reg 9 isn't working for everyone, usually Tier II [nations]," said Melville."
What might help with this issue is the development of a player's association with some real teeth – one that has a platform covering how many games should be players over a 12-month period, and how long down time should be. There are moves in the USA for a player's association, but that won't address the international question.


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|Topic Review (Newest First)
|Yes, I think I will stick with the vet for now, i dont want interferance with his other meds.loki lost almost 2 kilos, but he is eating alot and drinking, and having formed stools. I do believe the Doc mentioned panacur? So we will try that for 10 days. He is on clavamox for 4 days more, and he has prednisone for a month for his joints. And yes, the steroids are lowering his immune system. Definitely a huge clean down of the apartment. We havent been going out for walks other than potty outside, and a 2 block walk to my dog walkers place where I board him over night and I pick him up in the morn after work. Then Im ofc for a week so I can spend time nursing him back to health.
If he's on one abx. for the pocket of fluid, then I would be hesitant to put on another drug anyhow...how much longer on the current abx.?
Giardia resides in people and animals. It isn't always a critical issue. Although the GI issue from the possible parvo could factor in...but then the drugs could weaken the system too.
What abx. is he currently on?...Kocci may mean other parasite drugs. Maybe e-mail them
|I mean no disrespect to sincere advice given in this thread. But I would continue to work with your vet. I would be overly cautious veering away from the treatment plan the vet has advised.
|Looked up Kocci free, definitely would like to try it. But it says cant use it while on other antibiotics. Loki is on an antibiotic for that pocket of bacterial fluid in his abdominal wall. Will have to stuck with the vet meds for now, then I will try kocci free. I hope it wont enduce diarrhea. loki is having formed stools right now
the reason that you do more than one test with giardia is because the cysts aren't present in each and every test -- you may end up with false negatives. Multiple testing is the only guarantee for an accurate read.
don't skip this step
I would suggest you pass on the meds from the vet. You will end up on a cycle of loose poop, more tests, more fear...
Do a search on here for Kocci free. No side effects and This has worked for many on here where drugs failed...and I mean rounds and rounds and changes of meds. and tests and on and on. Even when fecal was negative, given meds anyhow and diarrhea cont'd...Kocci Free (follow dosing/timeline specifically) and bingo...no more issues.
Also want to consider Seacure for gastrointestinal repair and nutrient absorption due to the parvo. predigested fish protein and is absorbed directly without having to tax the liver and pancreas. Amino acid complex food.
Sorry to double post, I couldnt edit my post. Unfortunately Im at work today and tomorow the vet is closed for sunday and I can pick up the meds (I forgot the name they told me on the phone) on Monday morning at earliest. They told me its a 10 day dose with a poop sample in between and Im assuming after.
But Guys, I dont get this...10 day dose. and "between" poop sample. Why arent they giving me a 14 day dose with just a sample in the end of this period? Is the Vet trying to fish more money out of me? I have already spent 4000, and I would spend whatever to help heal my pup, but I dont want to be victimized with unnecessary tests. Its close to 60 for each poop test.
Im glad Im finding the source of his skininess. We did a poop sample a month ago and it came negative, so either Loki recently acquired it, or that specific sample didnt contain those buggers. Thing is, Loki has been having regular formed stools, until this incident, nor does did his belly look big so I never suspected. Oh please let this be the last of it. Im waiting for the c+s results from his joints, I dont want to hear another problem.
|Ugh. Poop results came back. loki has Giardia. Explains the skinniness. Says can be passed on to humans. Will need to bleach everything now
I agree with the ProPlan sensitive skin stomach. I used it for quite awhile with great results. They did put on alittle weight too.
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Your vet has to report it, or at least the vet who treated your dog. Do you have a written report. Ask for copies of all records from all who dealt with your pups condition.
Please put your dog a natural diet. He needs ALL the nutrition (natural enzymes and amino acids) he can get to repair cell damage.
Now here is a possibility that happened. Your pups first shots were knocked out by maternal antibodies (no one can predict when this will happen) leaving your pup vulnerable to parvo...you bring your pup in for more shots...the most likely place you are going to catch parvo is...AT THE VET. Inoculations supress the immune system for an estimated 10 days...once again leaving your pup vulnerable to disease.
The fecal tested positive for parvo.
The joint swelling, I truly believe was a vaccine reaction. The highest risk vaccine is Lepto. Lepto is a bacteria, not a virus.
I am happy he is home with you.
Consider the list Moms provided for holistic vets.
Kneebone is on O'Connor Dr. (Danforth area), in Toronto Mckutcheon (sp.), the owner of clinic has been in practice for 50yrs. (wrote the book "The New Holistic Way")
The Holistic Vet (North East Vet clinic) is up in Newmarket...The Owner of that practice went to California - Autumn Drouin DVM for over 30 yrs., still does consults at the clinic when up in Canada...Hyatt - the practice owner now.
Read their Bio here:
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LAMDA success
Ten pupils have been successful in the London Academy of Music and Dramatic Art Public Speaking examination. They each had to make 2 prepared speeches and deliver an impromtu speech on a given topic.
John Mak (Rhetoric:Distinction)
Morenikeji Awani (Rhetoric: Distinction)
Fabian Twist (Rhetoric:Distinction)
Laura Erel (Poetry: Distinction)
Jonathan Hallam (Poetry: Distinction)
Michelle D'Souza (Poetry: Merit)
James Whatham (Lower Grammar: Merit)
Ferdinand Floto (Poetry: Merit)
Erik Tullberg (Poetry: Merit)
Darren Chin (Lower Grammar: Pass)